The KLF7/PFKL/ACADL axis modulates cardiac metabolic remodelling during cardiac hypertrophy in male mice

Cao Wang, Shupei Qiao, Yufang Zhao, Hui Tian, Wei Yan, Xiaolu Hou, Ruiqi Wang, Bosong Zhang, Chaofan Yang, Fuxing Zhu, Yanwen Jiao, Jiaming Jin, Yue Chen and Weiming Tian ()
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Cao Wang: Harbin Institute of Technology
Shupei Qiao: Harbin Medical University
Yufang Zhao: Harbin Institute of Technology
Hui Tian: Harbin Institute of Technology
Wei Yan: The First Affiliated Hospital of Harbin Medical University
Xiaolu Hou: The Fourth Affiliated Hospital of Harbin Medical University
Ruiqi Wang: Harbin Institute of Technology
Bosong Zhang: Harbin Institute of Technology
Chaofan Yang: Harbin Institute of Technology
Fuxing Zhu: Harbin Institute of Technology
Yanwen Jiao: Harbin Institute of Technology
Jiaming Jin: Harbin Institute of Technology
Yue Chen: Harbin Institute of Technology
Weiming Tian: Harbin Institute of Technology

Nature Communications, 2023, vol. 14, issue 1, 1-18

Abstract: Abstract The main hallmark of myocardial substrate metabolism in cardiac hypertrophy or heart failure is a shift from fatty acid oxidation to greater reliance on glycolysis. However, the close correlation between glycolysis and fatty acid oxidation and underlying mechanism by which causes cardiac pathological remodelling remain unclear. We confirm that KLF7 simultaneously targets the rate-limiting enzyme of glycolysis, phosphofructokinase-1, liver, and long-chain acyl-CoA dehydrogenase, a key enzyme for fatty acid oxidation. Cardiac-specific knockout and overexpression KLF7 induce adult concentric hypertrophy and infant eccentric hypertrophy by regulating glycolysis and fatty acid oxidation fluxes in male mice, respectively. Furthermore, cardiac-specific knockdown phosphofructokinase-1, liver or overexpression long-chain acyl-CoA dehydrogenase partially rescues the cardiac hypertrophy in adult male KLF7 deficient mice. Here we show that the KLF7/PFKL/ACADL axis is a critical regulatory mechanism and may provide insight into viable therapeutic concepts aimed at the modulation of cardiac metabolic balance in hypertrophied and failing heart.

Date: 2023
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DOI: 10.1038/s41467-023-36712-9

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